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弥合差距:一种连接炎症与癌症的核因子κB调节因子

Bridging the Gap: A Regulator of NF-κB Linking Inflammation and Cancer.

作者信息

Postler Thomas S, Ghosh Sankar

机构信息

Department of Microbiology & Immunology, Columbia University, College of Physicians & Surgeons, New York, NY 10032, USA.

出版信息

J Oral Biosci. 2015 Aug 1;57(3):143-147. doi: 10.1016/j.job.2015.05.001.

Abstract

BACKGROUND

A close connection between inflammation and cancer has now been firmly established. While tumor initiation is typically independent of inflammatory events, immune cells infiltrating the tumor microenvironment secrete inflammatory cytokines that enhance the aberrant growth of tumor cells and thus facilitate tumor progression. Therefore, inflammation and tumor growth are usually interpreted as closely related on a systemic level but as distinct, independently regulated processes at a molecular level.

HIGHLIGHT

Recently, we reported that a sub-class of small GTPases, namely κB-Ras1 and κB-Ras2, regulate both inflammation tumor growth, thereby providing a unique molecular bridge between the two biological processes.

CONCLUSION

Here, we briefly summarize the known contact points between inflammation and cancer, including oral cancers, and put into context the identification of κB-Ras proteins as molecular link between two independent pathways important for tumor growth.

摘要

背景

炎症与癌症之间的紧密联系现已得到确凿证实。虽然肿瘤起始通常独立于炎症事件,但浸润肿瘤微环境的免疫细胞会分泌炎性细胞因子,这些因子会增强肿瘤细胞的异常生长,从而促进肿瘤进展。因此,炎症与肿瘤生长在系统层面通常被解读为密切相关,但在分子层面则是截然不同、独立调节的过程。

亮点

最近,我们报道了一类小GTP酶,即κB-Ras1和κB-Ras2,它们同时调节炎症和肿瘤生长,从而在这两个生物学过程之间提供了一个独特的分子桥梁。

结论

在此,我们简要总结炎症与癌症(包括口腔癌)之间已知的联系点,并将κB-Ras蛋白作为对肿瘤生长重要的两条独立途径之间的分子联系这一发现置于相应背景中。

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